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Uhm, Tae-Kyoung, Ki-Seung Kim, Yu-Deok Seo, and Sung-Kie Youn. "T-spline Finite Element Method for CAD/CAE Integrated Approach." Transactions of the Korean Society of Mechanical Engineers A 33, no. 2 (2009): 127–34. http://dx.doi.org/10.3795/ksme-a.2009.33.2.127.
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Netto, Jeffrey, Andrej Teren, Ralph Burkhardt, et al. "Biomarkers for Non-Invasive Stratification of Coronary Artery Disease and Prognostic Impact on Long-Term Survival in Patients with Stable Coronary Heart Disease." Nutrients 14, no. 16 (2022): 3433. http://dx.doi.org/10.3390/nu14163433.
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Knowledge about cardiac and inflammatory biomarkers in patients with stable coronary artery disease (CAD) is limited. To address this, we analyzed 3072 patients (36% female) with a median follow-up of 10 years in the Leipzig LIFE Heart Study with suspected CAD with coronary angiography. Selected biomarkers included troponin T (hsTNT), N-terminal pro B-type natriuretic peptide (NT-proBNP), copeptin, C-reactive protein (hsCRP), and interleukin-6 (IL-6). Patients were stratified by CAD severity: CAD0 (no sclerosis), CAD1 (non-obstructive, i.e., stenosis < 50%), and CAD2 (≥one stenosis ≥ 50%). Group comparison (GC) included GC1: CAD0 + 1 vs. CAD2; GC2: CAD0 vs. CAD1 + 2. CAD0, CAD1, and CAD2 were apparent in 1271, 631, and 1170 patients, respectively. Adjusted for classical risk factors, hs-cTnT, NT-proBNP, and IL-6 differed significantly in both GC and hsCRP only in GC2. After multivariate analysis, hs-cTnT, NT-proBNP, and IL-6 remained significant in GC1. In GC2, hs-cTnT (p < 0.001) and copeptin (p = 0.014) reached significance. Ten-year survival in groups CAD0, CAD1, and CAD2 was 88.3%, 77.3%, and 72.4%. Incorporation of hs-cTnT, NT-proBNP, copeptin, and IL-6 improved risk prediction (p < 0.001). The studied cardiac and inflammatory biomarkers enable fast and precise non-invasive identification of mortality risk in CAD patients, allowing the tailoring of primary and secondary CAD prevention.
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Lloyd, Peter, Colin C. McAndrew, Michael J. McLennan, et al. "Technology CAD at AT&T." Microelectronics Journal 26, no. 2-3 (1995): 79–97. http://dx.doi.org/10.1016/0026-2692(95)98915-e.
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Baltrūnienė, Vaida, Ieva Rinkūnaitė, Julius Bogomolovas, et al. "The Role of Cardiac T-Cadherin in the Indicating Heart Failure Severity of Patients with Non-Ischemic Dilated Cardiomyopathy." Medicina 56, no. 1 (2020): 27. http://dx.doi.org/10.3390/medicina56010027.
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Background and objectives: T-cadherin (T-cad) is one of the adiponectin receptors abundantly expressed in the heart and blood vessels. Experimental studies show that T-cad sequesters adiponectin in cardiovascular tissues and is critical for adiponectin-mediated cardio-protection. However, there are no data connecting cardiac T-cad levels with human chronic heart failure (HF). The aim of this study was to assess whether myocardial T-cad concentration is associated with chronic HF severity and whether the T-cad levels in human heart tissue might predict outcomes in patients with non-ischemic dilated cardiomyopathy (NI-DCM). Materials and Methods: 29 patients with chronic NI-DCM and advanced HF were enrolled. Patients underwent regular laboratory investigations, echocardiography, coronary angiography, and right heart catheterization. TNF-α and IL6 in serum were detected by enzyme-linked immunosorbent assay (ELISA). Additionally, endomyocardial biopsies were obtained, and the levels of T-cad were assessed by ELISA and CD3, CD45Ro, CD68, and CD4- immunohistochemically. Mean pulmonary capillary wedge pressure (PCWP) was used as a marker of HF severity, subdividing patients into two groups: mean PCWP > 19 mmHg vs. mean PCWP < 19 mmHg. Patients were followed-up for 5 years. The study outcome was composite: left ventricular assist device implantation, heart transplantation, or death from cardiovascular causes. Results: T-cad shows an inverse correlation with the mean PCWP (rho = −0.397, p = 0.037). There is a tendency towards a lower T-cad concentration in patients with more severe HF, as indicated by the mean PCWP > 19 mmHg compared to those with mean PCWP ≤ 19 mmHg (p = 0.058). Cardiac T-cad levels correlate negatively with myocardial CD3 cell count (rho = −0.423, p = 0.028). Conclusions: Univariate Cox regression analysis did not prove T-cad to be an outcome predictor (HR = 1, p = 0.349). However, decreased T-cad levels in human myocardium can be an additional indicator of HF severity. T-cad in human myocardium has an anti-inflammatory role. More studies are needed to extend the role of T-cad in the outcome prediction of patients with NI-DCM.
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Fukuda, Shiro, Shunbun Kita, Kazuya Miyashita, et al. "Identification and Clinical Associations of 3 Forms of Circulating T-cadherin in Human Serum." Journal of Clinical Endocrinology & Metabolism 106, no. 5 (2021): 1333–44. http://dx.doi.org/10.1210/clinem/dgab066.
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Abstract Context T-cadherin (T-cad) is a glycosylphosphatidylinositol (GPI)-anchored cadherin that mediates adiponectin to induce exosome biogenesis and secretion, protect cardiovascular tissues, promote muscle regeneration, and stimulate therapeutic heart protection by transplanted mesenchymal stem cells. CDH13, the gene locus of T-cad, affects plasma adiponectin levels most strongly, in addition to affecting cardiovascular disease risk and glucose homeostasis. Recently, it has been suggested that T-cad exists in human serum, although the details are still unclear. Objective To validate the existence of T-cad forms in human serum and investigate the association with clinical parameters of type 2 diabetes patients. Methods Using newly developed monoclonal antibodies against T-cad, pooled human serum was analyzed, and novel T-cad enzyme-linked immunosorbent assays (ELISAs) were developed. The serum T-cad concentrations of 183 Japanese type 2 diabetes patients were measured in a cross-sectional observational study. The main outcome measure was the existence of soluble T-cad in human serum. Results There were 3 forms of soluble T-cad: a 130-kDa form with a prodomain, a 100-kDa mature form, and a 30-kDa prodomain in human serum. Using newly developed ELISAs to measure them simultaneously, we found that the 130-kDa form of T-cad positively correlated with plasma adiponectin (r = 0.28, P &lt; .001), although a physiological interaction with adiponectin was not observed in serum. The unique 30-kDa prodomain was associated with several clinical parameters in diabetes patients. Conclusion We identified 3 novel forms of soluble T-cad. Their importance as disease markers and/or biomarkers of adiponectin function and the possible bioactivity of the respective molecules require further investigation.
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Philippova, Maria, Danila Ivanov, Manjunath B. Joshi, et al. "Identification of Proteins Associating with Glycosylphosphatidylinositol- Anchored T-Cadherin on the Surface of Vascular Endothelial Cells: Role for Grp78/BiP in T-Cadherin-Dependent Cell Survival." Molecular and Cellular Biology 28, no. 12 (2008): 4004–17. http://dx.doi.org/10.1128/mcb.00157-08.
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ABSTRACT There is scant knowledge regarding how cell surface lipid-anchored T-cadherin (T-cad) transmits signals through the plasma membrane to its intracellular targets. This study aimed to identify membrane proteins colocalizing with atypical glycosylphosphatidylinositol (GPI)-anchored T-cad on the surface of endothelial cells and to evaluate their role as signaling adaptors for T-cad. Application of coimmunoprecipitation from endothelial cells expressing c-myc-tagged T-cad and high-performance liquid chromatography revealed putative association of T-cad with the following proteins: glucose-related protein GRP78, GABA-A receptor α1 subunit, integrin β3, and two hypothetical proteins, LOC124245 and FLJ32070. Association of Grp78 and integrin β3 with T-cad on the cell surface was confirmed by surface biotinylation and reciprocal immunoprecipitation and by confocal microscopy. Use of anti-Grp78 blocking antibodies, Grp78 small interfering RNA, and coexpression of constitutively active Akt demonstrated an essential role for surface Grp78 in T-cad-dependent survival signal transduction via Akt in endothelial cells. The findings herein are relevant in the context of both the identification of transmembrane signaling partners for GPI-anchored T-cad as well as the demonstration of a novel mechanism whereby Grp78 can influence endothelial cell survival as a cell surface signaling receptor rather than an intracellular chaperone.
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Khanna, Roopali, Avinash Bansal, Sudeep Kumar, et al. "Association between Endogenous Sex Hormones and Coronary Artery Disease in Postmenopausal Women." Indian Journal of Cardiovascular Disease in Women - WINCARS 06, no. 03 (2021): 168–73. http://dx.doi.org/10.1055/s-0041-1736250.
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Background Incidence of coronary artery disease (CAD) increases significantly in postmenopausal women, which is assumed to be an imbalance between serum androgen and estrogen levels. However, studies assessing serum sex hormones and CAD are few and have shown conflicting results. Objective To compare serum sex hormone levels and traditional risk factors among postmenopausal women with angiographically proven CAD and without CAD. Method The study included consecutive postmenopausal women undergoing coronary angiography in our institute from May 2016 to June 2017. The clinical and coronary angiographic data and traditional risk factors were assessed. Fasting serum levels of estradiol (E2), testosterone (T), sex hormone-binding globulin (SHBG), dehydroepiandrosterone sulfate (DHEA-S), and insulin were measured. Results A total of 121 postmenopausal women were included in the study; 69 were CAD and 52 without CAD. Single-vessel disease was most common (55.1%), followed by double-vessel disease (24.6%) and triple-vessel disease (20.3%). Women with CAD had significantly lower estradiol/testosterone (E2/T) ratio (3.7 ± 2.6 vs. 5.4 ± 4.2, p = 0.008) compared with non-CAD group. SHBG, DHEA-S, and insulin levels were similar in CAD and non-CAD groups. The serum level of estradiol predicted the E2/T ratio (r = 0.316, p < 0.001) and positively associated with DHEA (r = 0.181, p = 0.047). Testosterone was negatively associated with E2/T ratio (r = – 0.682, p < 0.001). There was no significant correlation of estrogen, testosterone, or E2/T ratio to lipid profile (total cholesterol, HDL, LDL) in women with CAD. Conclusion E2/T ratio was significantly lowered in postmenopausal women with CAD. E2/T ratio may be a used a predictor of CAD in postmenopausal women
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Labay, V. A., and J. Bornemann. "CAD of T-septum waveguide evanescent-mode filters." IEEE Transactions on Microwave Theory and Techniques 41, no. 4 (1993): 731–33. http://dx.doi.org/10.1109/22.231675.
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Foster, Jeffrey C. "CAE/CAD at AT&T: An Introduction." AT&T Technical Journal 70, no. 1 (1991): 2–8. http://dx.doi.org/10.1002/j.1538-7305.1991.tb00493.x.
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Abu-Amero, Khaled K., Carol A. Wyngaard, and Nduna Dzimiri. "Prevalence and Role of Methylenetetrahydrofolate Reductase 677 C→T and 1298 A→C Polymorphisms in Coronary Artery Disease in Arabs." Archives of Pathology & Laboratory Medicine 127, no. 10 (2003): 1349–52. http://dx.doi.org/10.5858/2003-127-1349-paromr.
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Abstract Context.—Previous studies reported an association of 677 C→T and 1298 A→C methylenetetrahydrofolate reductase (MTHFR) variants with coronary artery disease (CAD). No previous studies concerning the prevalence of these 2 MTHFR variants or their possible association with CAD in Arabs are currently available in the literature. Objective.—To determine the prevalence of MTHFR variants and their potential relevance to CAD among Arabs. Design.—We used polymerase chain reaction and restriction enzyme digestion to determine the prevalence of these 2 MTHFR polymorphisms in 625 healthy blood donors (BDs) and 545 angiographically confirmed CAD patients of Arab origin. Results.—For the 677 C→T variant within the CAD group, 64.2% were homozygous wild-type C/C, 32.1% were heterozygous C/T, and 3.7% were homozygous T/T genotype. Within the BD group tested for the 677 C→T variant, 72.2% were homozygous wild-type C/C, 25.8% were heterozygous C/T, and 2% were homozygous T/T genotype. Within the CAD group tested for the 1298 A→C variant (n = 540), 45.7% were homozygous wild-type A/A, 46.9% were heterozygous A/C, and 7.4% were homozygous C/C genotype. Within the BD group tested for the 1298 A→C variant (n = 625), 39.4% were homozygous wild-type A/A, 51.5% were heterozygous A/C, and 9.1% were homozygous C/C genotype. The distribution and allele frequency of these 2 MTHFR variants followed the Hardy-Weinberg equilibrium and were similar in the CAD and BD study groups. The prevalence of the 677 C→T and 1298 A→C compound heterozygosity was 9.6% for the BD group and 12.3% for the CAD group. Conclusion.—The 2 MTHFR variants tested in this study, individually or compound, are not associated with CAD. Therefore, neither of these 2 variants can be considered an independent risk factor or a predictor for CAD in this population.
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Joshi, Manjunath B., Danila Ivanov, Maria Philippova, Emmanouil Kyriakakis, Paul Erne, and Thérèse J. Resink. "A requirement for thioredoxin in redox-sensitive modulation of T-cadherin expression in endothelial cells." Biochemical Journal 416, no. 2 (2008): 271–80. http://dx.doi.org/10.1042/bj20080765.
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T-cad (T-cadherin), a glycosylphosphatidylinositol-anchored cadherin superfamily member, is expressed widely in the brain and cardiovascular system, and absent, decreased, or even increased, in cancers. Mechanisms controlling T-cad expression are poorly understood. The present study investigated transcriptional regulation of T-cad in ECs (endothelial cells). Conditions of oxidative stress (serum-deprivation or presence of H2O2) elevate T-cad mRNA and protein levels in ECs. Reporter gene analysis, using serially deleted T-cad promoter stretches ranging from −99 to −2304 bp, located the minimal promoter region of T-cad within −285 bp from the translation start site. Reporter activity in ECs transfected with the −285 bp construct increased under conditions of oxidative stress, and this was normalized by antioxidant N-acetylcysteine. An electrophoretic-mobility-shift assay revealed a specific nucleoprotein complex unique to −156 to −203 bp, which increased when nuclear extracts from oxidatively stressed ECs were used, suggesting the presence of redox-sensitive binding element(s). MS analysis of the nucleoprotein complex unique to −156 to −203 bp after streptavidin–agarose pull-down detected the presence of the redox-active protein thioredoxin. The presence of thioredoxin-1 in a nuclear extract from oxidatively stressed ECs was demonstrated after immunoprecipitation and immunoblotting. Transfection of ECs with thioredoxin-1 small interfering RNA abrogated oxidative-stress-induced up-regulation of T-cad transcripts and protein. We conclude that thioredoxin-1 is an important determinant of redox-sensitive transcriptional up-regulation of T-cad in ECs.
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Guerrero, Julien, Boris Dasen, Agne Frismantiene, et al. "T-cadherin Expressing Cells in the Stromal Vascular Fraction of Human Adipose Tissue: Role in Osteogenesis and Angiogenesis." Stem Cells Translational Medicine 11, no. 2 (2022): 213–29. http://dx.doi.org/10.1093/stcltm/szab021.
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Abstract Cells of the stromal vascular fraction (SVF) of human adipose tissue have the capacity to generate osteogenic grafts with intrinsic vasculogenic properties. However, cultured adipose-derived stromal cells (ASCs), even after minimal monolayer expansion, lose osteogenic capacity in vivo. Communication between endothelial and stromal/mesenchymal cell lineages has been suggested to improve bone formation and vascularization by engineered tissues. Here, we investigated the specific role of a subpopulation of SVF cells positive for T-cadherin (T-cad), a putative endothelial marker. We found that maintenance during monolayer expansion of a T-cad-positive cell population, composed of endothelial lineage cells (ECs), is mandatory to preserve the osteogenic capacity of SVF cells in vivo and strongly supports their vasculogenic properties. Depletion of T-cad-positive cells from the SVF totally impaired bone formation in vivo and strongly reduced vascularization by SVF cells in association with decreased VEGF and Adiponectin expression. The osteogenic potential of T-cad-depleted SVF cells was fully rescued by co-culture with ECs from a human umbilical vein (HUVECs), constitutively expressing T-cad. Ectopic expression of T-cad in ASCs stimulated mineralization in vitro but failed to rescue osteogenic potential in vivo, indicating that the endothelial nature of the T-cad-positive cells is the key factor for induction of osteogenesis in engineered grafts based on SVF cells. This study demonstrates that crosstalk between stromal and T-cad expressing endothelial cells within adipose tissue critically regulates osteogenesis, with VEGF and adiponectin as associated molecular mediators.
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Turner, Michael J., C. Siddiq Abdul-Alim, Richard A. Willis, Terrence L. Fisher, Edith M. Lord, and John G. Frelinger. "T-cell antigen discovery (T-CAD) assay: a novel technique for identifying T cell epitopes." Journal of Immunological Methods 256, no. 1-2 (2001): 107–19. http://dx.doi.org/10.1016/s0022-1759(01)00436-7.
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Song, Xingfa, Haidong Wang, Chao Wang, et al. "Association of Sirtuin Gene Polymorphisms with Susceptibility to Coronary Artery Disease in a North Chinese Population." BioMed Research International 2022 (February 18, 2022): 1–8. http://dx.doi.org/10.1155/2022/4294008.
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Aims. Coronary artery disease (CAD) represents the leading cause of death worldwide. Accumulating evidence also suggests that sirtuins (SIRTS) have been associated with CAD. The present study was aimed at investigating the association between 12 gene polymorphisms for SIRTs and the development of CAD in a Chinese population. Materials and Methods. 12 SNPs (rs12778366 ( T > C ), rs3758391 ( T > C ), rs3740051 ( A > G ), rs4746720 ( C > T ), rs7895833 ( G > A ), rs932658 ( A > C ) for SIRT1, rs2015 ( G > T ) for SIRT2, rs28365927 ( G > A ), rs11246020 ( C > T ) for SIRT3, rs350844 ( G > A ), rs350846 ( G > C ), and rs107251 ( C > T ) for SIRT6) were selected and assessed in a cohort of 509 CAD patients and 552 matched healthy controls for this study. Genomic DNA from whole blood was extracted, and the SNPs were assessed using MassARRAY method. Results. TT genotype for rs3758391 and GG genotype for rs7895833 of SIRT1 were at higher risk of CAD, whereas the CC genotype for rs4746720 of SIRT1 was associated with a significantly decreased risk of CAD. The A allele of the rs28365927 of SIRT3 showed a significant decreased risk association with CAD patient group ( P = 0.014 ). Significant difference in genotypes rs350844 ( G > A ) ( P = 0.004 ), rs350846 ( G > C ) ( P = 0.002 ), and rs107251 ( C > T ) ( P ≤ 0.01 ) for SIRT6 was also found between the CAD patients and the healthy controls. Haplotype CTA significantly increased the risk of CAD ( P = 0.000118 , OR = 1.497 , 95 % CI = 1.218 – 1.840 ), while haplotype GCG significantly decreases the risk of CAD ( P = 0.000414 , OR = 1.131 , 95 % CI = 0.791 – 1.619 ). Conclusions. The SNP rs28365927 in the SIRT3 gene and SNP rs350844, rs350846, and rs107251 in the SIRT6 gene present significant associations with CAD in a north Chinese population. Haplotype CTA and GCG generated by rs350846/rs107251/rs350844 in the SIRT6 might also increase and decrease the risk of CAD, respectively.
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Ko, Eun-Ju, In-Jai Kim, Jeong-Yong Lee, et al. "Study of the Association between VEGF Polymorphisms and the Risk of Coronary Artery Disease in Koreans." Journal of Personalized Medicine 12, no. 5 (2022): 761. http://dx.doi.org/10.3390/jpm12050761.
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Coronary artery disease (CAD), a leading cause of death worldwide, has a complex etiology comprising both traditional risk factors (type 2 diabetes, dyslipidemia, arterial hypertension, and cigarette smoking) and genetic factors. Vascular endothelial growth factor (VEGF) notably contributes to angiogenesis and endothelial homeostasis. However, little is known about the relationship between CAD and VEGF polymorphisms in Koreans. The aim of this study is to investigate the associations of 2 VEGF promoter region polymorphisms (−1154G>A [rs1570360], −1498T>C [rs833061]) and 4 VEGF 3′-UTR polymorphisms (+936C>T [rs3025039], +1451C>T [rs3025040], +1612G>A [rs10434], and +1725G>A [rs3025053]) with CAD susceptibility in Koreans. We studied 885 subjects: 463 CAD patients and 422 controls. Genotyping was conducted with polymerase chain reaction-restriction fragment length polymorphism analysis and TaqMan allelic discrimination assays, and the genotype frequencies were calculated. We then performed haplotype and genotype combination analyses and measured the associations between VEGF polymorphisms and clinical variables in both the CAD patients and control subjects. We detected statistically significant associations between CAD and certain VEGF allele combinations. In the haplotypes of 5 single-nucleotide polymorphisms, the VEGF allele combination −1154A/+936T was associated with a decreased prevalence of CAD (A-T-T-G-G of VEGF −1154G>A/−1498T>C/+936C>T/+1612G>A/+1725G>A, AOR = 0.077, p = 0.021). In contrast, the VEGF allele combinations −1498T/+1725A and −1498T/+1612A/+1725A were associated with an increased prevalence of CAD (G-T-C-C-A of VEGF −1154G>A/−1498T>C/+936C>T/+1451C>T/+1725G>A, AOR = 1.602, p = 0.047; T-C-C-A-A of VEGF −1498T>C/+936C>T/+1451C>T/+1612G>A/+1725G>A, AOR = 1.582, p = 0.045). Gene–environment combinatorial analysis showed that the combination of the VEGF +1725AA genotype and several clinical factors (e.g., body mass index, hemoglobin A1c, and low-density lipoprotein cholesterol) increased the risk of CAD. Therefore, we suggest that VEGF polymorphisms and clinical factors may impact CAD prevalence.
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Saigusa, Ryosuke, Jenifer Vallejo, Rishab Gulati, et al. "Sex Differences in Coronary Artery Disease and Diabetes Revealed by scRNA-Seq and CITE-Seq of Human CD4+ T Cells." International Journal of Molecular Sciences 23, no. 17 (2022): 9875. http://dx.doi.org/10.3390/ijms23179875.
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Despite the decades-old knowledge that males and people with diabetes mellitus (DM) are at increased risk for coronary artery disease (CAD), the reasons for this association are only partially understood. Among the immune cells involved, recent evidence supports a critical role of T cells as drivers and modifiers of CAD. CD4+ T cells are commonly found in atherosclerotic plaques. We aimed to understand the relationship of CAD with sex and DM by single-cell RNA (scRNA-Seq) and antibody sequencing (CITE-Seq) of CD4+ T cells. Peripheral blood mononuclear cells (PBMCs) of 61 men and women who underwent cardiac catheterization were interrogated by scRNA-Seq combined with 49 surface markers (CITE-Seq). CAD severity was quantified using Gensini scores, with scores above 30 considered CAD+ and below 6 considered CAD−. Four pairs of groups were matched for clinical and demographic parameters. To test how sex and DM changed cell proportions and gene expression, we compared matched groups of men and women, as well as diabetic and non-diabetic subjects. We analyzed 41,782 single CD4+ T cell transcriptomes for sex differences in 16 women and 45 men with and without coronary artery disease and with and without DM. We identified 16 clusters in CD4+ T cells. The proportion of cells in CD4+ effector memory cluster 8 (CD4T8, CCR2+ Em) was significantly decreased in CAD+, especially among DM+ participants. This same cluster, CD4T8, was significantly decreased in female participants, along with two other CD4+ T cell clusters. In CD4+ T cells, 31 genes showed significant and coordinated upregulation in both CAD and DM. The DM gene signature was partially additive to the CAD gene signature. We conclude that (1) CAD and DM are clearly reflected in PBMC transcriptomes, and (2) significant differences exist between women and men and (3) between subjects with DM and non-DM.
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Bytyçi, Ibadete, Liliana Alves, Oscar Alves, Carla Lopes, Gani Bajraktari, and Michael Y. Henein. "Left Ventricular Myocardial and Cavity Velocity Disturbances Are Powerful Predictors of Significant Coronary Artery Stenosis." Journal of Clinical Medicine 11, no. 20 (2022): 6185. http://dx.doi.org/10.3390/jcm11206185.
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Background and Aim: Dobutamine stress echocardiography (DSE) is a well-established noninvasive investigation for significant coronary artery disease (CAD). The aim of this study was to evaluate the accuracy of cardiac Doppler parameters in predicting CAD. Methods: We prospectively studied 103 consecutive patients with suspected CAD based on typical symptoms; 59 proved to have CAD, and 44 patients proved to have no-CAD (n = 44). All patients underwent a complete stress Doppler echocardiographic examination. Total isovolumic time (T-IVT) as a marker of cavity dyssynchrony and wall motion score index (WMSI) were also calculated. Results: At peak dobutamine stress, the compromised LV longitudinal excursion (MAPSE), systolic septal and lateral velocities (s’), and diastolic indices were more pronounced in the CAD patients compared with those without CAD, but LV dimension did not differ between groups (p > 0.05). The WMSI was higher and t-IVT more prolonged in patients with CAD (p < 0.01 for both). Similarly, the changes were more pronounced in patients with significant CAD compared with insignificant CAD. On multivariate model, Δ mean s’, OR 2.016 (1.610 to 3.190; p < 0.001), Δ E velocity OR 2.502 (1.179 to 1.108; p < 0.001), Δ t-IVT 2.206 (1.180 to 2.780; p < 0.001) and Δ WMSI OR 1.911 (1.401 to 3.001; p = 0.001) were the most powerful independent predictors of the presence of CAD, particularly when significant (>75%). Δ mean s’ < 5.0 was 85% sensitive, 89% specific with AUC 0.92. Respective values for Δ E velocity <6.0 cm/s were 82%, 90% and 0.91; for Δ t-IVT > 4.5, 78%, 77% and 0.81 and for Δ FT ≥ 150 ms, 76%, 78% and 0.84 in predicating significant CAD. WMSI ≥ 0.7 was 75% sensitive, 77% specific with AUC of 0.81 in predicting significant CAD. The accuracy of DSE was higher in significant CAD compared to insignificant CAD (80% vs. 74%; p = 0.03). Conclusions: Compromised LV longitudinal systolic function, lower delta E wave, prolonged t-IVT, and increased WMSI were the most powerful independent predictors of the presence and significance of CAD. These finding strengthen the role of comprehensive DSE analysis in diagnosing ischemic disturbances secondary to significant CAD.
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MASUDA, Hiroo. "Trends of Simulation Technolgies. T-CAD and Its Application." Journal of Japan Institute of Electronics Packaging 2, no. 3 (1999): 188–93. http://dx.doi.org/10.5104/jiep.2.188.
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Boyer-Nancy, B. "Le CAD améliore-t-il les performances en détection ?" Imagerie de la Femme 14, no. 2 (2004): 75–84. http://dx.doi.org/10.1016/s1776-9817(04)94787-6.
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Dong, Mengzhen, Shousheng Liu, Mengke Wang, Yifen Wang, Yongning Xin, and Shiying Xuan. "Relationship between AGT rs2493132 polymorphism and the risk of coronary artery disease in patients with NAFLD in the Chinese Han population." Journal of International Medical Research 49, no. 7 (2021): 030006052110192. http://dx.doi.org/10.1177/03000605211019263.
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Objective To investigate the relationship between angiotensin ( AGT) rs2493132 gene polymorphism and the risk of developing non-alcoholic fatty liver disease (NAFLD) and coronary artery disease (CAD) in the Chinese Han population. Methods Polymerase chain reaction was performed to determine AGT genotypes. Anthropometric and clinical data were investigated and statistically analyzed in the clinical laboratory department of Qingdao Municipal Hospital. Results The AGT rs2493132 CT + TT genotype was an important risk factor for CAD in patients with NAFLD and NAFLD + CAD in healthy controls. The AGT rs2493132 T allele increased the risk of NAFLD + CAD in healthy controls. The AGT rs2493132 CT + TT genotype and T allele also significantly increased the risk of CAD in patients with NAFLD after adjustments for age, sex, and body mass index. In addition, AGT rs2493132 T allele carriers showed higher total cholesterol (TC) and low-density lipoprotein (LDL) levels compared with non-carriers. Conclusions The AGT rs2493132 CT + TT genotype and T allele significantly increased the risk of developing CAD in patients with NAFLD in the Chinese Han population. The AGT rs2493132 T allele was associated with increased serum TC and LDL levels.
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Juilliére, Yves, Mirande Candito, Charles E. Adjalla, et al. "Association of MTRR A66G polymorphism (but not of MTHFR C677T and A1298C, MTR A2756G, TCN C776G) with homocysteine and coronary artery disease in the French population." Thrombosis and Haemostasis 94, no. 09 (2005): 510–15. http://dx.doi.org/10.1160/th05-04-0262.
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Summarymethylenetetrahydrofolate reductase polymorphism (MTHFR C677T) is an established determinant of homocysteine plasma level (t-Hcys) while its association with coronary artery disease (CAD) seems to be more limited. In contrast, the association of the substitutions A2756G of methionine synthase (MTR), A66G of methionine synthase reductase (MTRR) and C776G of transcobalamin (TCN) to both t-Hcys and CAD needs to be evaluated further. The objective was to evaluate the association of these polymorphisms with t-Hcys and CAD in a French population. We investigated the individual and combined effects of these polymorphisms and of vitamin B12 and folates with t-Hcys in 530 CAD patients and 248 matched healthy controls. t-Hcys was higher in the CAD group than in controls (11.8 vs 10.4 μM, P<0.0001) and in carriers of MTRR AA and MTHFR 677TT than in those carrying the most frequent allele of both polymorphisms (13.8 vs 11.4 μM, P=0.0102 and 12.5 vs 11.0 mM, P=0.0065 respectively). The frequency of MTRR A allele was higher in CAD patients than in controls (0.48 [95% CI: 0.44-0.52] vs 0.38 [95% CI: 0.32-0.44], P=0.0081) while no difference was observed for MTHFR 677T frequency. In multivariate analysis, t-Hcys > median and MTRR AA genotype were two significant independent predictors of CAD with respective odds ratios of 3.1 (95 % CI: 1.8-5.1, P<0.0001) and 4.5 (95% CI: 1.5-13.1, P=0.0051). In conclusion, in contrast to North Europe studies, MTRR AA genotype is a genetic determinant of moderate hyperhomocysteinemia associated with CAD in a French population without vitamin fortification.
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Jha, Chandan K., Rashid Mir, Imadeldin Elfaki, et al. "Evaluation of the Association of Omentin 1 rs2274907 A>T and rs2274908 G>A Gene Polymorphisms with Coronary Artery Disease in Indian Population: A Case Control Study." Journal of Personalized Medicine 9, no. 2 (2019): 30. http://dx.doi.org/10.3390/jpm9020030.
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Coronary artery disease (CAD) is a major cause of death all over the world. CAD is caused by atherosclerosis which is induced by the interaction of genetic factors and environmental factors. Traditional environmental risk factors include hyperlipidemia, diabetes mellitus, lack of exercise, obesity, poor diet and others. Genome-wide association studies have revealed the association of certain gene polymorphisms with susceptibility to CAD. Omentin 1 is an adipokine secreted by the visceral adipose tissues and has been reported to have anti-inflammatory, cardioprotective, and enhances insulin sensitivity. In this study, we examined the role of omentin-1 common single nucleotide polymorphisms (SNPs) (rs2274907 A>T and rs2274908 G>A) in CAD. We genotyped 100 CAD patients and 100 matched healthy controls from the south Indian population using an amplification refractory mutation system (ARMS-PCR) and allele-specific PCR (AS-PCR). Our result indicated the rs2274908 G>A is not associated with CAD. Results showed that there was a significant difference in rs2274907 A>T genotype distribution between controls and CAD cases (P-value < 0.05). Results indicated that the AT genotype of the rs2274907 is associated with CAD with OR = 3.0 (95% confidence interval (CI), 1.64 to 5.49), 1.65 (1.27 to 2.163), P = 0.002. The T allele of the rs2274907 was also associated with CAD with OR = 1.82 (95% CI, 1.193 to 2.80), 1.37 (1.08 to 1.74), P = 0.005. Rs2274907 genotype distribution was also correlated with serum total cholesterol, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), hypertension and diabetes. We conclude that the AT genotype and the T allele of the rs2274907 A>T is associated with Cad in the south Indian population. Further studies on the effect of the rs2274907 A>T on omentin-1 function are recommended, and future well-designed studies with larger sample sizes and in different populations are required to validate our findings.
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Jha, Chandan K., Rashid Mir, Imadeldin Elfaki, et al. "Reply to Comment: Evaluation of the Association of Omentin 1 rs2274907 A > T and rs2274908 G > A Gene Polymorphisms with Coronary Artery Disease in Indian Population: A Case–Control Study." Journal of Personalized Medicine 10, no. 4 (2020): 194. http://dx.doi.org/10.3390/jpm10040194.
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Coronary artery disease (CAD) is a major cause of death all over the world. CAD is caused by atherosclerosis which is induced by the interaction of genetic factors and environmental factors. Genome-wide association studies have revealed the association of certain gene polymorphisms with susceptibility to CAD. Omentin 1 is an adipokine secreted by the visceral adipose tissues and has been reported to have anti-inflammatory, cardioprotective, and enhances insulin sensitivity. In this study, we examined the role of omentin-1 common single nucleotide polymorphisms (SNPs) (rs2274907 A > T and rs2274908 G > A) in CAD. We conclude that the AT genotype and the T allele of the rs2274907 A > T is associated with Cad in the south Indian population. Our results indicated that the rs2274907 SNP may be associated with CAD in this population. This finding needs further validation in well-designed and large-sample size studies before being introduced in clinical settings.
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Mir, Rashid, Chandan k. Jha, Imadeldin Elfaki, et al. "Incidence of MicroR-4513C/T Gene Variability in Coronary Artery Disease - A case-Control Study." Endocrine, Metabolic & Immune Disorders - Drug Targets 19, no. 8 (2019): 1216–23. http://dx.doi.org/10.2174/1871530319666190417111940.
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Background: Genetic variants in pre-microRNA genes or the 3'UTR of miRNA target genes could influence miRNA-mediated regulation of gene expression and thus contribute to the susceptibility and prognosis of human diseases. Several studies have investigated the association of genetic variants in the seed region of miRNAs with cardiometabolic phenotypes .Therefore the aim of study was to investigate the potential association of miR-4513 rs2168518 C>T gene variability with the risk of developing CAD and its association with different cardiometabolic phenotypes in an Indian cohort to stratify CAD burden in the general population. Methods: The study was conducted on 100 clinically confirmed CAD patients and 100 healthy individuals. Genotyping of MicroR-4513 rs2168518C>T gene variability was performed using Amplification refractory mutation system PCR method. Results: A significant difference was observed in the genotype distribution among CAD cases and healthy controls. The frequencies of three genotypes CC, CT, TT in CAD patient and healthy controls were 5%, 77%, 18%, and 28%, 45% and 27% respectively. A multivariate analysis showed that miR- 4513 rs2168518 polymorphism is associated with an increased susceptibility to CAD in codominant inheritance model for variant CC vs. CT OR 9.58 CI (3.45-26.57), RR 2.3(1.75-3.02), P=0.001. Results also indicate a potential dominant effect of miR-4513 rs2168518 C/T polymorphism on susceptibility of CAD in dominant inheritance model for variant CC vs. (CT+TT) OR 7.38 (2.71-20.07), RR 1.96 (1.56-2.46), P=0.001. In allelic comparison, T allele weakly increased risk of CAD compared to C allele (OR=1.50, 95% CI (1.09-2.26) RR 1.15 (0.94-1.39) P=0.044. Conclusion: It is concluded that CT genotype and T allele of microR-4513 rs2168518 is strongly associated with increased susceptibility to CAD. Furthers studies with larger sample sizes are necessary to confirm this result.
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Malisuwan, S., J. Sivaraks, P. Promkladpanao, and Y. Thamachareon. "CAD Model and Simulation of T-Shaped Microstrip Antenna for LTE 1800MHz Applications." International Journal of Future Computer and Communication 3, no. 5 (2014): 354–57. http://dx.doi.org/10.7763/ijfcc.2014.v3.326.
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Popova, A. A., I. N. Shubin, and R. E. Aliev. "CALS Technologies in Mechanical Engineering Using the Example of Developing Three-Dimensional Models of Typical Products." Vestnik Tambovskogo gosudarstvennogo tehnicheskogo universiteta 26, no. 4 (2020): 637–49. http://dx.doi.org/10.17277/vestnik.2020.04.pp.637-649.
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Three-dimensional models of the body parts were developed using the basic 3D modeling operations (rotation, extrusion, threading, etc.) of the T-FLEX CAD 3D CAD system, which made it possible to significantly simplify the work with assembly 3D models representing a complex structure consisting of a large number of parts. During the trial operation, the advantages of using the T-FLEX CAD 3D CAD system have been proven when working with complex 3D models. The advantages of using the program in the machine-building cluster are shown.
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Zhou, Liting, Lin Xie, Dongchun Zheng, et al. "Genetic Variants of CD40 Gene Are Associated with Coronary Artery Disease and Blood Lipid Levels." BioMed Research International 2016 (2016): 1–8. http://dx.doi.org/10.1155/2016/1693619.
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Objectives. The present study aimed to evaluate the effect ofCD40andCXCR4genes polymorphisms on CAD susceptibility and the blood lipid levels and history of cardiovascular risk factors in a Chinese Han population.Materials and Methods. A total of 583 unrelated patients with CAD and 540 controls were recruited. Two tag SNPs (rs4239702 and rs1535045) at theCD40locus and one tag SNP (rs2228014) at theCXCR4locus were genotyped using the SEQUENOM Mass-ARRAY system.Results. After adjusting the risk factors, the frequency of rs1535045-T allele was also higher in patients than controls. Haplotype analysis showed that the rs4239702(C)-rs1535045(T) haplotype was associated with CAD. People with rs4239702-TT genotype had higher blood lipid levels in case group while it was not in the control group. History of cardiovascular risk factors showed no association for the three SNPs in case group and control group.Conclusions. rs1535045 inCD40gene is likely to be associated with CAD in the Chinese Han population. rs4239702(C)-rs1535045(T) haplotype was associated with CAD. Only in CAD patients, the blood lipid level of patients with rs4239702-TT genotype was higher than other patients.CXCR4gene may not relate to CAD.
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Wang, Haidong, Chao Wang, Xingfa Song, Hai Liu, Yun Zhang, and Pei Jiang. "Association of FKBP5 polymorphisms with patient susceptibility to coronary artery disease comorbid with depression." PeerJ 8 (June 3, 2020): e9286. http://dx.doi.org/10.7717/peerj.9286.
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Background Coronary artery disease (CAD) and depression cause great burden to society and frequently co-occur. The exact mechanisms of this comorbidity are unclear. FK506-binding protein 51 (FKBP51) is correlated with cardiovascular disease and depression. The aim of this study was to determine the role of the seven single nucleotide polymorphisms (SNPs) of FKBP5 that code FKBP51, namely, rs1360780 (C>T), rs2817032 (T>C), rs2817035 (G>A), rs9296158 (G>A), rs9470079 (G>A), rs4713902 (T>C), and rs3800373 (C>T) in a patient’s susceptibility to comorbid CAD and depression. Methods We enrolled 271 Northern Chinese Han patients with CAD, including 123 patients with depression and 147 patients without depression. We also included 113 healthy controls that match the patients’ sex and age. Genomic DNA from whole blood was extracted, and seven SNPs were assessed using MassArray method. Patient Health Questionnaire-9 was applied to access the depression. Results The GA genotype for rs9470079 was associated with a significantly decreased risk of CAD (odds ratio = 0.506, 95% confidence interval = 0.316–0.810, P = 0.005) when the GG genotype was used as reference. A statistically significant difference was observed among females but not among males in the rs9470079 genotype and allele frequency. Patients with CAD were further divided into CAD+D and CAD-D groups according to the presence of comorbid depression and were compared with the controls. Significant differences were found regarding the genotype and allele frequency of rs2817035 and rs9470079 in CAD+H groups compared with the control subjects in all groups and the female groups (P < 0.05). Conclusions The current study found a remarkable association between FKBP5 gene variations and the risk of comorbid CAD and depression in a north Chinese population. rs9470079 may be a potential gene locus for the incidence of comorbid CAD and depression.
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Ma, Xiaowei, Jia Huang, Difei Lu, et al. "Genetic Variability of the Glucose-Dependent Insulinotropic Peptide Gene Is Involved in the Premature Coronary Artery Disease in a Chinese Population with Type 2 Diabetes." Journal of Diabetes Research 2018 (March 25, 2018): 1–7. http://dx.doi.org/10.1155/2018/6820294.
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Background. Glucose-dependent insulinotropic polypeptide (GIP) is closely related to diabetes and obesity, both of which are confirmed to increase the risk of coronary artery disease (CAD). Our study aimed to investigate whether the polymorphisms in GIP genes could affect the risk of cardiovascular disease in type 2 diabetic patients in the Chinese Han population. Methods. We selected and genotyped two haplotype-tagging single nucleotide polymorphisms (tag-SNPs) (rs2291725 C>T, rs8078510 G>A) of GIP gene based on CHB data in HapMap Phase II database (r2<0.8). The case-control study of Chinese Han population involved 390 diabetic patients with CAD as positive group and 276 diabetic patients without CAD as control group. Allele and genotype frequencies were compared between the two groups. Results. In dominant inheritance model, the carriers of T/T or T/C had a lower risk of CAD (OR = 0.635, 95% CI = 0.463–0.872, p=0.005), even after adjustment other CAD risk factors (gender, age, BMI, smoking status, dyslipidemia, hypertension history, and diabetic duration) (OR′ = 0.769, 95% CI′ = 0.626–0.945, p′=0.013). The allele A at rs8078510 was associated with decreased risk of CAD (OR = 0.732, p=0.039). p=0.018 in subgroup analysis, individuals with higher BMI (≥24 kg/m2) had increased risk for CAD when carrying C/C at rs2291725 (OR′ = 1.291, 95% CI′ = 1.017–1.639, p′=0.036). In age < 55 men and age < 65 women, the carriers of allele C at rs2291725 had a higher risk of CAD than noncarriers (OR = 1.627, p=0.015). Carriers of allele G in rs8078510 had higher susceptibility to CAD (OR = 2.049, 95% = CI 1.213–3.463, p=0.007). p=0.004; in addition, allele G in rs8078510 would bring higher CAD risk to the carriers who ever smoked (OR = 1.695, 95% CI = 1.080–2.660, p=0.021). Conclusion. The genetic variability of GIP gene is associated with CAD and it may play a role in the premature CAD in the Chinese Han population with type 2 diabetes.
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Elwazir, Mohamed Y., Mohammad H. Hussein, Eman A. Toraih, et al. "Association of Angio-LncRNAs MIAT rs1061540/MALAT1 rs3200401 Molecular Variants with Gensini Score in Coronary Artery Disease Patients Undergoing Angiography." Biomolecules 12, no. 1 (2022): 137. http://dx.doi.org/10.3390/biom12010137.
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Long non-coding RNAs (lncRNAs) have emerged as essential biomolecules with variable diagnostic and/or prognostic utility in several diseases, including coronary artery disease (CAD). We aimed for the first time to investigate the potential association of five angiogenesis-related lncRNAs (PUNISHER, SENCR, MIAT, MALAT1, and GATA6-AS) variants with CAD susceptibility and/or severity. TaqMan Real-Time genotyping for PUNISHER rs12318065A/C, SENCR rs12420823C/T, MIAT rs1061540C/T, MALAT1 rs3200401T/C, and GATA6-AS1 rs73390820A/G were run on the extracted genomic DNA from 100 unrelated patients with stable CAD undergoing diagnostic coronary angiography and from 100 controls. After adjusting covariates, the studied variants showed no association with disease susceptibility; however, MIAT*T/T genotype was associated with a more severe Gensini score. In contrast, MALAT1*T/C heterozygosity was associated with a lower score. The lipid profile, and to a lesser extent smoking status, male sex, weight, hypertension, and MALAT1 (T > C) (negative correlation), explained the variance between patients/control groups via a principal component analysis. Incorporating the principal components into a logistic regression model to predict CAD yielded a 0.92 AUC. In conclusion: MIAT rs1061540 and MALAT1 rs3200401 variants were associated with CAD severity and Gensini score in the present sample of the Egyptian population. Further large multi-center and functional analyses are needed to confirm the results and identify the underlying molecular mechanisms.
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Liu, Qing-Li, Hiroyuki Kishi, Kenzo Ohtsuka, and Atsushi Muraguchi. "Heat shock protein 70 binds caspase-activated DNase and enhances its activity in TCR-stimulated T cells." Blood 102, no. 5 (2003): 1788–96. http://dx.doi.org/10.1182/blood-2002-11-3499.
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AbstractDNA fragmentation is a hallmark of cells undergoing apoptosis and is mediated mainly by the caspase-activated DNase (CAD or DNA-fragmentation factor 40 [DFF40]), which is activated when released from its inhibitor protein (ICAD or DFF45) upon apoptosis signals. Here we analyzed the effect of heat shock protein 70 (Hsp70) on CAD activity in T-cell receptor (TCR)–induced apoptosis using a T-cell line (TAg-Jurkat). Overexpression of Hsp70 significantly augmented the apoptotic cell death as well as DNA fragmentation in CD3/CD28- or staurosporine-stimulated cells. Following stimulation of cells with CD3/CD28 or staurosporine, Hsp70 was coprecipitated with free CAD, but not with CAD associated with ICAD. Furthermore, the purified Hsp70 dose-dependently augmented DNA-fragmentation activity of caspase-3–activated CAD in a cell-free system. Peptide-binding domain–deleted Hsp70 could neither bind nor augment its activity, while adenosine triphosphate (ATP)–binding domain–deleted Hsp70 or the peptide-binding domain itself bound CAD and augmented its activity. These results indicate that the the binding of Hsp70 to the activated CAD via the peptide-binding domain augments its activity. Although CAD lost its activity in an hour after being released from ICAD in vitro, its activity was retained after an hour of incubation in the presence of Hsp70, suggesting that Hsp70 may be involved in stabilization of CAD activity. Finally, CAD that had been coprecipitated with Hsp70 from the cell lysate of staurosporine-activated 293T cells induced chromatin DNA fragmentation and its activity was not inhibited by ICAD. These results suggest that Hsp70 binds free CAD in TCR-stimulated T cells to stabilize and augment its activity.
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JANCIN, BRUCE. "Troponin T Test May Help Spot Risk in Stable CAD." Family Practice News 38, no. 11 (2008): 11. http://dx.doi.org/10.1016/s0300-7073(08)70704-7.
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Hansen, U., and S. B�ttgenbach. "T-CAD for the analysis and verification of processing sequences." Microsystem Technologies 10, no. 3 (2004): 193–98. http://dx.doi.org/10.1007/s00542-003-0348-1.
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Kim, In-Jai, Jeong-Yong Lee, Hyeon-Woo Park, et al. "Association between HOTAIR lncRNA Polymorphisms and Coronary Artery Disease Susceptibility." Journal of Personalized Medicine 11, no. 5 (2021): 375. http://dx.doi.org/10.3390/jpm11050375.
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Coronary artery disease (CAD), one of the most frequent causes of mortality, is the most common type of cardiovascular disease. This condition is characterized by the accumulation of plaques in the coronary artery, leading to blockage of blood flow to the heart. The main symptom of CAD is chest pain caused by blockage of the coronary artery and shortness of breath. HOX transcript antisense RNA gene (HOTAIR) is a long non-coding RNA which is well-known as an oncogene involved in various cancers, such as lung, breast, colorectal, and gastric cancer. We selected six single nucleotide polymorphisms, rs4759314 A>G, rs1899663 G>T, rs920778 T>C, rs7958904 G>C, rs12826786 C>T, and rs874945 C>T, for genotype frequency analysis and assessed the frequency of HOTAIR gene polymorphisms in 442 CAD patients and 418 randomly selected control subjects. To analyze the differences between these two populations, we performed a Student’s t-test, adjusted odds ratio (AOR), 95% confidence intervals (CIs), and ANOVA analysis. According to our baseline characteristic analysis, control subjects and CAD patients were significantly different in hypertension and diabetes mellitus. We also found that the rs4759314 A>G, rs1899663 G>T, and rs12826786 C>T genotypes were strongly associated with CAD susceptibility (AA vs. AG+GG: AOR = 0.608, 95% CI = 0.393−0.940, p = 0.025; GG vs. TT: AOR = 2.276, 95% CI = 1.125−4.607, p = 0.022; CC vs. CT+TT: AOR = 1.366, 95% CI = 1.027−1.818, p = 0.032, respectively). Our data also demonstrated that the genotype of HOTAIR polymorphisms, genotype combination, and haplotype analysis affect disease occurrence. Moreover, these polymorphisms are linked to clinical factors that contribute to disease susceptibility. In conclusion, results from our study suggest that HOTAIR polymorphisms may be useful novel biomarkers for diagnosing CAD.
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Mráz, Miloš, Anna Cinkajzlová, Jana Kloučková, et al. "Coronary Artery Disease Is Associated with an Increased Amount of T Lymphocytes in Human Epicardial Adipose Tissue." Mediators of Inflammation 2019 (February 7, 2019): 1–9. http://dx.doi.org/10.1155/2019/4075086.
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Immunocompetent cells including lymphocytes play a key role in the development of adipose tissue inflammation and obesity-related cardiovascular complications. The aim of the study was to explore the relationship between epicardial adipose tissue lymphocytes and coronary artery disease (CAD). To this end, we studied the content and phenotype of lymphocytes in peripheral blood, subcutaneous adipose tissue (SAT), and epicardial adipose tissue (EAT) in subjects with and without CAD undergoing elective cardiac surgery. Eleven subjects without CAD (non-CAD group) and 22 age-, BMI-, and HbA1C-matched individuals with CAD were included into the study. Blood, SAT, and EAT samples were obtained at the beginning of surgery. Lymphocyte populations were quantified as % of CD45+ cells using flow cytometry. Subjects with CAD had a higher total lymphocyte amount in EAT compared with SAT (32.24±7.45 vs. 11.22±1.34%, p=0.025) with a similar trend observed in non-CAD subjects (29.68±7.61 vs. 10.13±2.01%, p=0.067). T (CD3+) cells were increased (75.33±2.18 vs. 65.24±4.49%, p=0.032) and CD3- cells decreased (21.17±2.26 vs. 31.64±4.40%, p=0.028) in EAT of CAD relative to the non-CAD group. In both groups, EAT showed an elevated percentage of B cells (5.22±2.43 vs. 0.96±0.21%, p=0.039 for CAD and 12.49±5.83 vs. 1.16±0.19%, p=0.016 for non-CAD) and reduced natural killer (NK) cells (5.96±1.32 vs. 13.22±2.10%, p=0.012 for CAD and 5.32±1.97 vs. 13.81±2.72%, p=0.022 for non-CAD) relative to SAT. In conclusion, epicardial adipose tissue in subjects with CAD shows an increased amount of T lymphocytes relative to non-CAD individuals as well as a higher number of total and B lymphocytes and reduced NK cells as compared with corresponding SAT. These changes could contribute to the development of local inflammation and coronary atherosclerosis.
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Epstein, Rachel. "Prime models of computably enumerable degree." Journal of Symbolic Logic 73, no. 4 (2008): 1373–88. http://dx.doi.org/10.2178/jsl/1230396926.
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AbstractWe examine the computably enumerable (c.e.) degrees of prime models of complete atomic decidable (CAD) theories. A structure has degree d if d is the degree of its elementary diagram. We show that if a CAD theory T has a prime model of c.e. degree c, then T has a prime model of strictly lower c.e. degree b, where, in addition, b is low (b′ = 0′), This extends Csima's result that every CAD theory has a low prime model. We also prove a density result for c.e. degrees of prime models. In particular, if c and d are c.e. degrees with d < c and c not low2 (c″ > 0″), then for any CAD theory T, there exists a c.e. degree b with d < b < c such that T has a prime model of degree b, where b can be chosen so that b′ is any degree c.e. in c with d′ ≤ b′. As a corollary, we show that for any degree c with 0 < c < 0′, every CAD theory has a prime model of low c.e. degree incomparable with c. We show also that every CAD theory has prime models of low c.e. degree that form a minimal pair, extending another result of Csima. We then discuss how these results apply to homogeneous models.
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Kaur, Kulwinder, and Chandan Kumar Jha. "Identify the Significant Hypostatic or Epistatic Effect Between the Various SNPs of LDLR gene through SNP-SNP Interaction and Haplotype Analysis - A Case Control Study." International Journal of Health Sciences and Research 12, no. 8 (2022): 255–62. http://dx.doi.org/10.52403/ijhsr.20220834.
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The coronary artery disease (CAD) is a leading cause of the morbidity and mortality worldwide and has also become a major public health burden in India in recent decades. The LDLR gene mutations have been reported associated with familial CVD and are one of the main risk factors for developing coronary artery disease (CAD). In the present study using the contingency chi-square test, statistically significant differences were observed between the CAD cases and matched healthy controls in the distribution of the genotypes of four out six SNPs investigated viz., rs688C>T (p=0.0031), rs1529729C>T (p=0.0001), rs5925G>A (p=0.006) and rs72658855C>T (p=0.0349). This suggested that these four SNPs are associated with CAD in the present material studied from Bangalore. SNP-SNP interaction analysis revealed statistically significant hypostatic effect of rs688-rs2228671 combination, while rs688-rs72658855 combination showed statistically significant epistatic effect and the haplotype analysis demonstrated decreased (protective) risk of statistically significant association of TATCC, CGTCC and TACCT with CAD. Further studies from different regions of the country are required to validate the present findings relating the association of genomic variants of LDLR gene with the susceptibility to CAD in people of India. Key words: CAD-coronary artery disease; LDLR-low-density lipoprotein receptor; SNP-SNP interaction; Haplotype analysis; OR-odds ratio; CI-confidence interval .
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Гущина, А. Р., та Д. В. Гулякин. "Сравнительный анализ CAD-систем". ТЕНДЕНЦИИ РАЗВИТИЯ НАУКИ И ОБРАЗОВАНИЯ 93, № 9 (2023): 104–6. http://dx.doi.org/10.18411/trnio-01-2023-462.
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В данной статье рассматриваются легкие, средние и тяжѐлые уровни CAD систем. Каждый уровень отличается функциональностью и сложностью решений поставленных задач. Представлено краткое описание и отличительные черты таких CAD-систем, как AutoCAD, КОМПАС, NanoCAD, T-FLEX CAD, SolidWorks, CATIA. Рассмотрены отличия программ по основным функциям. Выяснено, что в наше время рынок полон различных программ, и существует возможность выбрать программу, подходящую по необходимым критериям.
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Wang, Y. Y., R. Su, B. C. Li, et al. "AB0269 THE CHARACTERISTICS OF PERIPHERAL LYMPHOCYTE SUBSETS AND CYTOKINES LEVEL IN RHEUMATOID ARTHRITIS WITH CORONARY ARTERY DISEASE." Annals of the Rheumatic Diseases 79, Suppl 1 (2020): 1433.1–1433. http://dx.doi.org/10.1136/annrheumdis-2020-eular.2754.
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Background:Rheumatoid arthritis (RA) is a systemic autoimmune disease. It is characterized by highly disabling polyarthritis, but extra-articular features are also common and portend a poor prognosis. Compared with the general population, the incidence and mortality of cardiovascular disease in RA are significantly increased. Chronic autoimmune inflammation is the common pathogenesis of RA and coronary heart disease(CAD). We’ve proved that lymphocyte subsets imbalance and high cytokines expression play an important role in the occurrence and development of RA diseases. However, the level of lymphocyte subsets and cytokines of RA patients with CAD are rarely reported[1-2].Objectives:To explore the clinical characteristic of lymphocyte subsets and cytokines of RA patients with CAD,and make comparisons with simple RA patients and healthy controls.Methods:The study included 96 patients with a diagnosis of RA according to the 1987 revised criteria of the ACR, including 54 RA patients with CAD and 42 RA patients without CAD and other cardiovascular disease, 40 healthy controls are also concluded. The absolute numbers of lymphocyte subsets and T subsets in peripheral blood were measured by Flow Cytometer (FCM). Serum levels of IL-2, IL-4, IL-6, IL-10, IL-17, INF-γ, and TNF-α were measured by flow microsphere capture chip technique (CBA) for 19 RA patients with CAD and 38 simple RA patients among 96 patients.We also collected relevant clinical information and made DAS28 score, and all patients are in the middle-high disease activity group (DAS28>3.2).Results:(1) There was no difference in DAS28 scores between the two groups(p=0.572). (2)Compared with RA patients without CAD, the absolute number of total T cell(P=0.035), total B cell (P=0.006), CD4+T cell(P=0.012), Th1 cell(P=0.037), Th17 cell(P=0.033) and CD4+CD25+FOXP3+ Treg(P=0.003) was lower than RA patients with CAD, the number of NK cell(P=0.685), CD8+T cell(P=0.322) and Th2 cell(P=0.770) had no obvious difference between them. (3)Compared with the healthy control, the absolute number of total T cell(P=0.014), total B cell (P=0.006), CD8+T cell(P=0.000) in RA with CAD was evidently lower, but there was no siginificant difference in absolute number of CD4+T cell(P=0.582), Th1 cell(P=0.052), Th2 cell(P=0.595), Th17 cell(P=0.148) and Treg(P=0.176) (Figure 1).(4) In RA patients with CAD,the level of cytokines IL-2(P=0.042), IL-4(P=0.043) and IL-17(P=0.012) was lower, while other cytokines had no difference (Table 1).Figure 1.The absolute number of lymphcytes of RA patients with CAD(n=54),RA patients without CAD (n=42) and healthy control (n=40). (*P<0.05,**P<0.01, ***P<0.001).Table 1.The expression level of cytokines of RA patients with CAD(n=19) and RA patients without CAD (n=38).Cytokines (pg/ml)RA and CAD group(A) (n = 19)RA group(B) (n = 38)PvalueA vs. BIL-25.50(1.96, 12.82)6.82(4.45, 14.44)0.042IL-44.93(1.67, 9.41)6.28(4.49, 11.88)0.043IL-623.69(10.93, 73.08)36.67(15.40, 72.50)0.636IL-107.76(4.54, 10.50)7.62(5.69, 19.91)0.223IL-1710.81(4.04, 20.25)20.68(13.88, 45.58)0.012IFN-γ6.10(3.27, 13.84)7.13(5.79, 15.83)0.115TNF-α10.49(2.50, 29.04)14.96(10.03, 30.39)0.097Conclusion:Our research shows that there is lymphocyte imbalance and immune disorder existing in RA patients with CAD. Both the number of lymphocyte subsets and cytokine levels decreased in these patients than pure RA patients. It suggests that this group may be in lower immune state, which providing guidance for further clinical treatment of RA patients with CAD.References:[1]Winchester R, Giles JT, Nativ S, et al. Association of Elevations of Specific T Cell and Monocyte Subpopulations in Rheumatoid Arthritis With Subclinical Coronary Artery Atherosclerosis. [J]. Arthritis Rheumatol, 2016,68(1): 92-102.[2]England BR, Thiele GM, Anderson DR, et al. Increased cardiovascular risk in rheumatoid arthritis: mechanisms and implications. [J]. BMJ, 2018 04 23;361.Disclosure of Interests:None declared
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Daoud, Mohamed S. "Variants of D9N, G188A, N291S, and 93 T/G Genes in patients with Coronary Artery Diseases." Medical Science and Discovery 8, no. 12 (2021): 698–705. http://dx.doi.org/10.36472/msd.v8i12.636.
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Objective: Our work aimed to study the relationship between LPL variants D9N, G188A, N291S, and 93 T/G genes and CAD in Saudi patients. Materials and Methods: We recruited 253 CAD patients, who underwent diagnostic coronary angiography, and 207 control subjects. Several biochemical and behavioral markers were obtained, and different genotypes of LPL variants, D9N, G188E, N291S, and 93 T/G, were detected using The PCR-RFLP method. Results: The current study found D9N genotypes, AA, AG, and GG in 71.14%, 23.72%, and 5.14% in CAD patients, respectively. the AA, AG, and GG control genotypes were found in 81.64%, 16.43%, and 1.93%, respectively. The OR of the D9N AA versus AG genotype with a 95% CI was determined to be 1.65 (1.04–2.65), (p = 0.035). The OR of the D9N AA versus AG + GG genotype with a 95% CI was 1.80 (1.16–2.81), (p = 0.009). A strong relation of the D9N AA was observed with CAD. For the G188E, N291S, 93T/G variants insignificant were observed in both CAD and control groups. Conclusion: This study revealed the D9N variant has an association with CAD; however, no relation was detected between CAD and G188E, N291S, and 93T/G variants in the Saudi patients.
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Valo, Misa, Annette Wons, Albert Moeller, and Claudius Teupe. "Markers of Myocardial Ischemia in Patients with Obstructive Sleep Apnea and Coronary Artery Disease." Pulmonary Medicine 2015 (2015): 1–6. http://dx.doi.org/10.1155/2015/621450.
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Obstructive sleep apnea (OSA) is characterized by intermittent hypoxia during sleep. We tested the hypothesis that nocturnal myocardial ischemia is detectable by ST segment depression and elevation of high sensitive troponin T (hsTrop T) and B-type natriuretic peptide (NT-proBNP) in patients with OSA and coexisting coronary artery disease (CAD). Twenty-one patients with OSA and CAD and 20 patients with OSA alone underwent in-hospital polysomnography. Blood samples for hsTrop T and NT-proBNP measurements were drawn before and after sleep. ST segment depression was measured at the time of maximum oxygen desaturation during sleep. The apnea-hypopnea-index (AHI), oxygen saturation nadir, and time in bed with oxygen saturation of ≤80% were similar in both groups. Levels of hsTrop T and NT-proBNP did not differ significantly before and after sleep but NT-proBNP levels were significantly higher in patients suffering from OSA and CAD compared to patients with OSA alone. No significant ST depression was found at the time of oxygen saturation nadir in either group. Despite the fact that patients with untreated OSA and coexisting CAD experienced severe nocturnal hypoxemia, we were unable to detect myocardial ischemia or myocyte necrosis based on significant ST segment depression or elevation of hsTrop T and NT-proBNP, respectively.
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Niessner, Alexander, Senta Graf, Mariam Nikfardjam, et al. "Circulating t-PA antigen predicts major adverse coronary events in patients with stable coronary artery disease – a 13-year follow-up." Thrombosis and Haemostasis 90, no. 08 (2003): 344–50. http://dx.doi.org/10.1160/th02-10-0185.
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SummaryThrombus formation after rupture of an atherosclerotic plaque plays a crucial role in coronary artery disease (CAD). A decreased endogenous fibrinolytic system and prothrombotic factors are supposed to influence coronary thrombosis. It was our aim to investigate the predictive value of tissue plasmino-gen activator (t-PA) antigen, von Willebrand Factor, Lipoprotein (a) and anti-cardiolipin antibodies for major adverse coronary events in patients with stable CAD in a prospective cohort study of more than 10 years.We observed 141 patients with angiographically proven CAD for a median follow-up period of 13 years. t-PA antigen was the only marker predicting coronary events (logistic regression, p = 0.044) with a poor prognosis for patients in the 5th quintile with an odds ratio of 7.3 (compared to the 1st quintile). The odds ratio even increased to 10.0 for coronary events associated with the “natural course” of CAD excluding events due to restenosis. t-PA antigen had a slightly higher prognostic power (ROC curve; AUC = 0.69) than fasting glucose (AUC = 0.68) and cholesterol (AUC = 0.67). Triglycerides influenced plasma levels of t-PA antigen (regression, p < 0.001). The predictive value of t-PA antigen remained significant after adjustment for inflammation (logistic regression, p = 0.013) and extent of CAD (p = 0.045) but disappeared adjusting for insulin resistance (p = 0.12).In conclusion t-PA antigen predicted coronary events during a very long-term follow-up with a comparable prognostic power to established cardiovascular risk factors. Markers of insulin resistance influenced t-PA antigen and its predictive value.Part of this paper was originally presented at the joint meetings of the 16th International Congress of the International Society of Fibrinolysis and Proteolysis (ISFP) and the 17th International Fibrinogen Workshop of the International Fibrinogen Research Society (IFRS) held in Munich, Germany, September 2002.
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Kebert, Cory B., June E. Eichner, William E. Moore, et al. "Relationship of the 1793G-A and 677C-T Polymorphisms of the 5,10-Methylenetetrahydrofolate Reductase Gene to Coronary Artery Disease." Disease Markers 22, no. 5-6 (2006): 293–301. http://dx.doi.org/10.1155/2006/825431.
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Numerous studies have investigated the relationship between polymorphisms, in particular 677C-T and 1298A-C, of the methylene-tetrahydrofolate reductase (MTHFR) gene and coronary artery disease (CAD) with conflicting results. This study investigates the potential association of two point mutations inMTHFR, 677C-T and 1793G-A, along with other risk factors, with CAD. This is the first hospital-based study to investigate 1793G-A in this context. Genotype analysis was performed on 729 Caucasians and 66 African Americans undergoing coronary angiography using a novel PCR-based assay involving formation of Holliday junctions. Allelic frequencies for 677C-T were 66.2% C and 33.8% T for Caucasians and 90.9% C and 9.1% T for African Americans. With respect to the 1793G-A polymorphism, allelic frequencies were 94.7% G and 5.3% A for Caucasians and 99.2% G and 0.8% A for African Americans. Disease associations were examined in the Caucasian patients due to their greater genotype variability and larger number in the patient cohort. Results suggest that neither 677CT heterozygotes (OR-1.36; 95% CI 0.95 to 1.96) nor mutant homozygotes (OR-0.73; 95% CI 0.44 to 1.20) have either an increased or decreased risk for CAD compared to the 677CC genotype. Likewise, the 1793GA genotype did not demonstrate a statistically significant association with CAD compared to 1793GG patients (OR-0.79; 95% CI 0.47 to 1.33). Mean homocysteine levels (μmol/L) increased from normal to mutant for 677C-T (677CC: 10.2; 677CT: 11.0; 677TT: 11.6) and normal to heterozygous in 1793G-A (1793GG: 10.7; 1793GA: 11.5). TheseMTHFRpolymorphisms did not contribute to the prediction of clinically defined CAD in Caucasians.
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Jha, Chandan K., Rashid Mir, Shaheena Banu, Imadeldin Elfaki, and Sukh M. S. Chahal. "Heterozygosity in LDLR rs2228671 and rs72658855 Gene is Associated with Increased Risk of Developing Coronary Artery Disease in India –A Case-Control Study." Endocrine, Metabolic & Immune Disorders - Drug Targets 20, no. 3 (2020): 388–99. http://dx.doi.org/10.2174/1871530319666191015164505.
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Objective: Coronary artery disease (CAD) is one of the most common causes of death worldwide. Risk factors of CAD include high LDL-C, low high-density lipoprotein (HDL), hypertension, lack of exercise, genetic factors, etc. Polymorphisms of the LDLR gene have been associated with CAD in previous studies. Methods: The LDLR-rs72658855 C>T genotyping was detected by using allele-specific PCR (ASPCR). The association of rs2228671 and rs72658855 with CAD in a south Indian cohort (200 CAD patients and 200 matched healthy controls was studied. Results: Our findings showed that rs2228671 gene variability is associated with increased susceptibility to coronary artery disease in the codominant inheritance model for variant CC vs. CT OR 3.42(1.09-10.7), with P<0.034. A non-significant association was reported in the recessive inheritance model for the variant (CC+CT) vs. TT OR 0.56(0.16-1.95), at P<0.36. and in the dominant inheritance model for variant CC vs. (CT+TT) OR 2.8(1.07-7.34), at P<0.032 .In case of allelic comparison, it was indicated that the LDLR rs2228671-T allele was associated with an increased risk of developing CAD <rs72658855 C>T gene variability was associated with an increased susceptibility to coronary artery disease in the codominant inheritance model for variant CC vs. CT OR 1.7(1.1-2.6), at P<0.015 and in the dominant inheritance model for variant CC vs. (CT+TT) OR 1.66(1.07-2.58), at P<0.0.02.. In case of allelic comparison, a non-significant association was reported in LDLR rs72658855-T and C allele. Conclusion: We concluded that the heterozygosity in LDLR-rs72658855 and rs2228671 and T allele in LDLR rs2228671 are strongly associated with increased susceptibility to coronary artery disease. These results must be validated by future well-designed studies with larger sample sizes and different populations.
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Kelle, Sebastian, Kelly Schlendorf, Glenn A. Hirsch, et al. "Gadolinium Enhanced MR Coronary Vessel Wall Imaging at 3.0 Tesla." Cardiology Research and Practice 2010 (2010): 1–9. http://dx.doi.org/10.4061/2010/856418.
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Purpose. We evaluated the influence of the time between low-dose gadolinium (Gd) contrast administration and coronary vessel wall enhancement (LGE) detected by 3T magnetic resonance imaging (MRI) in healthy subjects and patients with coronary artery disease (CAD).Materials and Methods.Four healthy subjects (4 men, mean age29 ± 3years and eleven CAD patients (6 women, mean age61±10years) were studied on a commercial 3.0 Tesla (T) whole-body MR imaging system (Achieva 3.0 T; Philips, Best, The Netherlands). T1-weighted inversion-recovery coronary magnetic resonance imaging (MRI) was repeated up to 75 minutes after administration of low-dose Gadolinium (Gd) (0.1 mmol/kg Gd-DTPA).Results.LGE was seen in none of the healthy subjects, however in all of the CAD patients. In CAD patients, fifty-six of 62 (90.3%) segments showed LGE of the coronary artery vessel wall at time-interval 1 after contrast. At time-interval 2, 34 of 42 (81.0%) and at time-interval 3, 29 of 39 evaluable segments (74.4%) were enhanced.Conclusion. In this work, we demonstrate LGE of the coronary artery vessel wall using 3.0 T MRI after a single, low-dose Gd contrast injection in CAD patients but not in healthy subjects. In the majority of the evaluated coronary segments in CAD patients, LGE of the coronary vessel wall was already detectable 30–45 minutes after administration of the contrast agent.
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Lu, Difei, Jia Huang, Xiaowei Ma, et al. "Rs46522 in the Ubiquitin-Conjugating Enzyme E2Z Gene Is Associated with the Risk of Coronary Artery Disease in Individuals of Chinese Han Population with Type 2 Diabetes." Journal of Diabetes Research 2017 (August 3, 2017): 1–5. http://dx.doi.org/10.1155/2017/4501794.
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Aims. We investigated the association between ubiquitin-conjugating enzyme E2Z (UBE2Z) gene SNP rs46522 and the risk of CAD in a Chinese Han population with type 2 diabetes and explored a possible interactive effect with environmental risk factors of CAD. Methods. 665 patients with T2D were enrolled; 390 were CAD patients and 275 were non-CAD patients. Genotype analysis of rs46522 (T>C) was performed using PCR-RFLP. Results. The SNP rs47522 was associated with the risk of CAD supposing recessive inheritance model (TT versus CC+CT, OR′=1.277, 95%CI′ 1.039–1.570, p′=0.020) and codominant model (TT versus CT, OR′=1.673, 95%CI′ 1.088–2.570, p′=0.019) after adjustment for confounders of CAD. A synergistic effect of rs46522 and BMI was discovered (β=0.012, p for interreaction = 0.028). In subgroup analysis, minor allele T was significantly associated with CAD in overweight and obesity subgroup (p=0.034), and the association was also proved in recessive model (OR=1.537, 95%CI 1.075–2.196, p=0.018). Smokers with genotype TT had threefold risk of CAD in comparison to nonsmokers with genotype TC or CC (p<0.001). Conclusions. The SNP rs46522 in UBE2Z gene is associated with the risk of CAD in the individuals of Chinese Han descent with type 2 diabetes and is of synergistic effect with BMI.
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Mir, Rashid, Imadeldin Elfaki, Jamsheed Javid, et al. "Genetic Determinants of Cardiovascular Disease: The Endothelial Nitric Oxide Synthase 3 (eNOS3), Krüppel-Like Factor-14 (KLF-14), Methylenetetrahydrofolate Reductase (MTHFR), MiRNAs27a and Their Association with the Predisposition and Susceptibility to Coronary Artery Disease." Life 12, no. 11 (2022): 1905. http://dx.doi.org/10.3390/life12111905.
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Coronary artery disease (CAD) is an important cause of death worldwide. CAD is caused by genetic and other factors including hypertension, hyperlipidemia, obesity, stress, unhealthy diet, physical inactively, smoking and Type 2 diabetes (T2D). The genome wide association studies (GWASs) have revealed the association of many loci with risk to diseases such as cancers, T2D and CAD. Nitric oxide (NO) is a potent vasodilator and is required for normal vascular health. It is produced in the endothelial cells in a reaction catalyzed by the endothelial NO synthase (eNOS). Methylenetetrahydrofolate reductase (MTHFR) is a very important enzyme involved in metabolism of folate and homocysteine, and its reduced function leads to cardiovascular disease. The Krüppel-like factor-14 (KLF-14) is an important transcriptional regulator that has been implicated in metabolic syndrome. MicroRNA (MiRNAs) are short non-coding RNAs that regulate the gene expression of proteins involved in important physiological processes including cell cycle and metabolism. In the present study, we have investigated the potential impact of germline pathogenic variants of endothelial eNOS, KLF-14, MTHFR, MiRNA-27a and their association with risk to CAD in the Saudi population. Methods: Amplification Refractory Mutation System (ARMS) PCR was used to detect MTHFR, KLF-14, miRNA-27a and eNOS3 genotyping in CAD patients and healthy controls. About 125 CAD cases and 125 controls were enrolled in this study and statistical associations were calculated including p-value, risk ratio (RR), and odds ratio (OD). Results: There were statistically significant differences (p < 0.05) in genotype distributions of MTHFR 677 C>T, KLF-14 rs972283 G>A, miRNAs27a rs895819 A>G and eNOS3 rs1799983 G>T between CAD patients and controls. In addition, our results indicated that the MTHFR-TT genotype was associated with increased CAD susceptibility with an OR 2.75 (95%) and p < 0.049, and the KLF14-AA genotype was also associated with increased CAD susceptibility with an OR of 2.24 (95%) and p < 0.024. Moreover, the miRNAs27a-GG genotype protects from CAD risk with an OR = 0.31 (0.016), p = 0.016. Our results also indicated that eNOS3 -GT genotype is associated with CAD susceptibility with an OR = 2.65, and p < 0.0003. Conclusion: The MTHFR 677C>T, KLF14 rs972283 G>A, miRNAs27a A>G, and eNOS3 rs1799983 G>T genotypes were associated with CAD susceptibility (p < 0.05). These findings require verification in future large-scale population based studies before these loci are used for the prediction and identification of individuals at risk to CAD. Weight control, physical activity, and smoking cessation are very influential recommendations given by clinicians to the at risk individuals to reduce or delay the development of CAD.
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Sitompul, Sanggap Indra, Budi Susetyo Pikir, Aryati, Citrawati Dyah Kencono Wungu, Shafira Kurnia Supandi, and Monika Estherlita Sinta. "Analysis of the Effects of IL-6 -572 C/G, CRP -757 A/G, and CRP -717 T/C Gene Polymorphisms; IL-6 Levels; and CRP Levels on Chronic Periodontitis in Coronary Artery Disease in Indonesia." Genes 14, no. 5 (2023): 1073. http://dx.doi.org/10.3390/genes14051073.
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Interleukin 6 (IL-6) and C-Reactive Protein (CRP) play an important role in chronic periodontitis with coronary artery disease (CAD). Genetic factors can affect a person’s risk of CAD, which affects one-third of the population. This study investigated the role of IL-6 -572 C/G, CRP -757 A/G, and CRP -717 T/C gene polymorphisms. IL-6 and CRP levels on the severity of periodontitis in CAD in Indonesia were also evaluated. This case-control study was conducted with mild and moderate–severe chronic periodontitis groups. A path analysis test was conducted with Smart PLS with a 95% confidence interval to determine the significant variable for chronic periodontitis. Our study revealed that the effects of IL-6 -572 C/G, CRP -757 A/G, and CRP -717 T/C gene polymorphisms on IL-6 levels and CRP levels were not significant. IL-6 and CRP levels were not significantly different between the two groups. We found that IL-6 levels had a significant effect on CRP levels in periodontitis patients with CAD (path coefficient 0.322, p = 0.003). IL-6 -572 C/G, CRP -757 A/G, and CRP -717 T/C gene polymorphisms had no effect on the severity of chronic periodontitis in CAD patients in the Indonesian population. We also observed no apparent effects of the influence of gene polymorphisms in IL-6 -572 C/G, CRP -757 A/G, and CRP -717 T/C genes. Although the IL-6 and CRP levels were not significantly different between the two groups, IL-6 levels affected CRP levels in periodontitis patients with CAD.
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Graf, Senta, Renate Beckmann, Stephan Hornykewycz, et al. "Fibrinolytic Response to Venous Occlusion Compared to Physical Stress Test in Young Patients with Coronary Artery Disease." Thrombosis and Haemostasis 82, S 01 (1999): 80–84. http://dx.doi.org/10.1055/s-0037-1615560.
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Summary Introduction: Venous occlusion (VO) and exercise stress (ES) are stimulators of the fibrinolytic system. Aim of this study was to answer which of both stimulation tests is more useful in patients with symptom-limited coronary artery disease (CAD) to evaluate possible defects in the fibrinolytic system. Methods and results: We investigated 20 patients (M/F = 15/5; mean age = 36.7 years) with angiographically proven CAD for their plasma levels of tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor-type-1 (PAI-1) at basal conditions as well as after VO and at maximal ES (standardised bicycle stress test) and compared the data to those obtained from 12 sex- and age-matched healthy controls (M/F = 9/3; mean age = 40.4 years). At basal conditions mean t-PA activity and t-PA antigen plasma levels were within the normal range and comparable between the two study groups. After both VO and maximal ES, mean t-PA activity and t-PA antigen levels increased significantly more in the control group as compared to the CAD group. Mean PAI-1 activity plasma levels were significantly higher in the CAD group at basal conditions before VO (patients 7.0 ± 3.1; controls 3.9 ± 3.9; IU/ml; p = 0.025) as well as before ES (patients 8.1 ± 3.5; controls 4.3 ± 3.8; IU/ml; p = 0.009). PAI-1 activity plasma levels showed a significant decrease for patients and controls only after VO, while PAI-1 activity was not significantly decreased in both study groups at maximal ES. Discussion: The significantly higher increase in mean plasma levels of t-PA activity and t-PA antigen after VO compared to ES in both groups might be explained by the fact that CAD induced symptoms in the patients during ES thus permitting only 80% of their age, sex, and body mass index related optimal work load. Conclusion: VO and ES are applicable triggers of the endogenous fibrinolytic system in healthy subjects and patients who are not limited in their physical exercise. Standardised VO appears to be superior to ES as stimulation test of the endogenous fibrinolytic system in patients with symptomatic CAD.
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Tung, Robert T. "Significance of New, Isolated T-wave Inversion in Multiple Electrocardiogram Leads with Regadenoson Injection in Patients with Normal Myocardial Perfusion Imaging." Kansas Journal of Medicine 12, no. 3 (2019): 80–82. http://dx.doi.org/10.17161/kjm.v12i3.11797.
Full textAbstract:

 Introduction
 The pharmacologic (regadenoson) stress myocardial perfusion imaging (MPI) is used widely in patients who cannot exercise for detecting coronary artery disease (CAD). The interpretation of these studies depends primarily on the imaging results because the sensitivity of electrocardiograms (ECG) in this setting is poor. Prior study showed that effects of regadenoson on ST-segment occurred infrequently and had low sensitivity for detecting CAD. The significance of T-wave inversion in multiple ECG leads without ST-segment depression with regadenoson injection in patients with normal MPI is described and reported.
 
 
 Methods
 ECGs were reviewed retrospectively in 64 patients who had regadenoson MPI and coronary angiography for evaluation of CAD from June 1, 2016 to August 31, 2018. Five cases were identified with new, isolated T-wave inversion in multiple ECG leads.
 
 
 Results
 All five cases had new and isolated T-wave inversion in multiple leads without ST segment depression with regadenoson injection and normal MPI. At coronary angiography, three of the five cases showed obstructive coronary artery disease who received coronary percutaneous intervention. One case had nonobstructive coronary artery disease and one had a normal coronary artery.
 
 
 Conclusions
 Despite nonspecific ST-T changes on baseline ECGs and normal MPI in all patients, three of five cases had obstructive CAD by coronary angiography. New, isolated T-wave inversion in multiple ECG leads with regadenoson injection were observed in our patients with normal MPI. These ECG findings may be associated with false negative MPI. Therefore, careful observation and scrutiny of all ECG changes, especially new, isolated T-wave inversion in multiple ECG leads during regadenoson MPI is advisable to identify potential obstructive CAD despite normal MPI findings.